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The role and therapeutic potential of nuclear factor κB (NF-κB) in ischemic stroke.
- Source :
-
Biomedicine & Pharmacotherapy . Feb2024, Vol. 171, pN.PAG-N.PAG. 1p. - Publication Year :
- 2024
-
Abstract
- Stroke is a prevalent cerebrovascular condition with a global impact, causing significant rates of illness and death. Despite extensive research, the available treatment options for stroke remain restricted. Hence, it is crucial to gain a deeper understanding of the molecular mechanisms associated with the onset and advancement of stroke in order to establish a theoretical foundation for novel preventive and therapeutic approaches. NF-κB, also known as nuclear factor κB, is a transcription factor responsible for controlling the expression of numerous genes and plays a crucial role in diverse physiological processes. NF-κB is triggered and regulates neuroinflammation and other processes after stroke, promoting the generation of cytokine storms and contributing to the advancement of ischemic stroke (IS). Therefore, NF-κB could potentially play a vital role in stroke by regulating diverse pathophysiological processes. This review provides an overview of the functions of NF-κB in stroke and its governing mechanisms. In addition, our attention is directed towards various potential therapies that aim to inhibit the NF-κB signaling pathway in order to offer valuable insights for the advancement of innovative treatment approaches for stroke. [Display omitted] ● NF-κB plays a key role in neuroinflammation following ischemic stroke. ● NF-κB is involved in regulating the pathological mechanisms of ischemic stroke. ● A series of therapies exert neuroprotective effects on ischemic stroke via inhibiting NF-κB signalling pathway. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 07533322
- Volume :
- 171
- Database :
- Academic Search Index
- Journal :
- Biomedicine & Pharmacotherapy
- Publication Type :
- Academic Journal
- Accession number :
- 175241042
- Full Text :
- https://doi.org/10.1016/j.biopha.2024.116140